Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Ganglionic Blockers”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 883 records · Page 49Linked to original sources
PubMed1999

Calcium channel subtypes differ at two types of cholinergic synapse in lumbar sympathetic neurones of guinea-pigs.

1. The involvement of different presynaptic Ca2+ channels in transmission at 'weak' (subthreshold) and 'strong' (suprathreshold) synapses was investigated in guinea-pig paravertebral ganglia isolated in vitro. Selective Ca2+ channel antagonists were used to block excitatory synaptic currents evoked by stimulating single preganglionic axons. 2. The N-type Ca2+ channel blocker, omega-conotoxin GVIA (100 nM), reduced peak synaptic conductance by similar amounts at weak synapses (by 39 +/- 6 %) and strong synapses (34 +/- 6 %). 3. The P-type Ca2+ channel blocker, omega-agatoxin IVA (40 nM), significantly reduced transmitter release at weak synapses (by 42 +/- 6 %) but had only a small effect at strong synapses (reduced by 6 +/- 2 %). 4. Blockers of Q-, L- or T-type Ca2+ channels had no significant effects on peak synaptic conductance at either type of synapse. 5. We conclude that the two functionally distinct types of preganglionic terminal in sympathetic ganglia which synapse on the same neurone differ in their expression of particular types of voltage-dependent Ca2+ channels. Both types utilize N-type channels and channels resistant to blockade by specific antagonists, but Ca2+ entry through P-type channels makes a substantial contribution to acetylcholine release only at weak synapses.

Animals↗
PubMed1964

THE GANGLION BLOCKING ACTION OF PROCAINAMIDE.

In cats and rabbits procainamide (20 to 50 mg, intravenously) produced a fall of blood pressure of 20 to 50 mm Hg which reached a maximal effect within 1 min and lasted for about 5 min. Procainamide reduced the pressor responses to nicotine and to carotid arterial occlusion and reduced the depressor response to vagal stimulation, but did not antagonize the actions of adrenaline or noradrenaline on blood vessels. The contractions of the nictitating membrane to stimulation of the preganglionic cervical sympathetic nerve were partially or completely blocked by 20 to 50 mg of procainamide given intravenously. The ganglion blocking effect was more abrupt in onset and more slow to recover than that due to hexamethonium and had about 1/250th of the activity of the latter. Procainamide (1 mg) reduced the acetylcholine output of the perfused superior cervical ganglion to below 30% of the control value and blocked transmission completely. Small doses (10 mug) reduced the acetylcholine output but hardly affected ganglionic transmission. Procainamide, injected into the perfused superior cervical ganglion, blocked contractions elicited by stimulation of the preganglionic cervical sympathetic nerve for a longer period than those produced by acetylcholine injected into the perfusion circuit to the ganglion; the reverse was true for hexamethonium. Procainamide reduced the size of action potentials recorded from the superior cervical ganglion without altering the resting potential of the ganglion. The ganglion blocking activities of procainamide and hexamethonium often potentiated each other, especially when the preparation had been set up for several hours. On the guinea-pig isolated ileum preparation, procainamide (0.5x10(-4) g/ml.) antagonized responses due to acetylcholine, histamine and, most effectively, to nicotine. On the isolated heart, procainamide (1 mg) almost abolished the bradycardia produced by acetylcholine; 10 mg slowed and weakened the heart, while 100 mg stopped it. We conclude that procainamide, like procaine, blocks ganglionic transmission by (1) depressing the release of acetylcholine from preganglionic nerve endings; and (2) competing, with the acetylcholine which is released, for receptor sites on the ganglion cells. The amounts required to produce significant effects in vivo and in vitro are comparable. The methods available for detecting this type of ganglion blocking action are discussed.

Acetylcholine↗
PubMed2002

Nicotinic acetylcholine receptors in autonomic ganglia.

Although alpha3beta4 subunit combination is clearly prevalent in the nAChRs of autonomic ganglia neurons, the ganglia are strikingly different in the ratio of neurons containing each particular nAChR subunit, as found with immunohistochemical methods and from the analysis of the effects of nAChR subunit-specific antibodies on the ACh-induced membrane currents. In particular, the number of neurons containing alpha3, alpha4, alpha5 or alpha7 subunits is by about three times higher in sympathetic ganglia than in parasympathetic ganglia. This difference may explain why the parasympathetic and sympathetic ganglia markedly differ in their pharmacology. Still, alpha7 subunit makes the highest contribution to ACh-induced membrane current. No correlation between the physiological functions of the ganglia and subunit composition of their nAChRs has been found as yet. High permeability for Ca2+ should permit the nAChRs with alpha7 subunits to influence a variety of Ca2+-dependent events in autonomic neurons. As found with biochemical methods and site-directed mutagenesis, the ACh binding site is formed in the alpha/beta subunits interface by multiple loops containing cysteine, tyrosine and tryptophan amino residues as important for ACh binding. Likewise, both alpha and beta subunits are important for the effects of blocking agents on nAChRs. As found by electrophysiological methods, each neuron of sympathetic and parasympathetic ganglia, as a rule, possesses nAChRs of two groups, "fast" and "slow", with the mean duration of the burst of single channel openings ranging approximately from 5 to 10 and from 25 to 45 ms, respectively. These groups of channels differ from each other with their pharmacology. The burst-like activity of autonomic nAChRs channels is possible only if the disulfide bonds are left intact, otherwise only single openings of the channel are observed. The ionic channel of a nAChRs pentamer is formed by M2 transmembrane segments arranging glutamate, serine, threonine, leucine, and valine rings critical for channel conductance and ionic selectivity. In particular, the mutations V251T and E237A, and insertion of proline or alanine, convert a cation-selective channel into an anion-selective one. The open-channel blockers bind to the nAChR channel at the level where the channel diameter is nearly 12 A, both for "fast" and "slow" channel groups.

Animals↗